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Jaroslav Denkovskij [1] and Edvardas Bagdonas [1] and Ilona Kusleviciute [1] and Zygmunt Mackiewicz [1] and Ausra Unguryte [1] and Narunas Porvaneckas [2] and Sandrine Fleury [3] and Algirdas Venalis [1] and Christian Jorgensen [4] and Eiva Bernotiene [1]

Academic Editor: Heinrich Sauer

1, Department of Regenerative Medicine, State Research Institute Centre for Innovative Medicine, Vilnius, Lithuania, imi.lt

2, Clinic of Rheumatology, Orthopaedics-Traumatology and Reconstructive Surgery, Vilnius University Faculty of Medicine, Vilnius, Lithuania, vu.lt

3, EFS Pyrénéés-Méditerranéé, Toulouse, France, sante.fr

4, INSERM U844, Hôpital Saint-Eloi and Hôpital Lapeyronie, Université Montpellier 1, Montpellier, France, univ-montp1.fr

Received Jan 24, 2017; Revised Apr 10, 2017; Accepted May 15, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Osteoarthritis (OA) is a slowly progressing joint disease, where the rate of loss of collagens and proteoglycans of cartilage matrix exceeds the rate of deposition of newly synthesized molecules [1]. Catabolism of matrix proteins can be accomplished by several classes of enzymes; however, the metalloproteinases (MMPs) are generally considered predominantly responsible for connective tissue destruction in arthritic joints [2, 3]. The activity of MMPs is controlled through the activation of proenzymatic form and the inhibition of active enzymes by tissue inhibitors of metalloproteinases (TIMPs). The contribution to cartilage degradation in arthritis has been suggested for the excess of MMPs over TIMPs [4]. The increased expression of MMP-1, MMP-3, and MMP-13, which degrades structural collagens, including intact collagen type II, in osteoarthritic cartilage suggests a major role for these enzymes in cartilage degradation [2]. Gelatinases A and B (MMP-2 and MMP-9, resp.) digest the denatured collagens, gelatins, as well as some noncollagen matrix components of the joints.

Many studies imply the therapeutic potential of mesenchymal stem cells (MSC) for cartilage repair in OA. Adipose tissue-derived stem cells (ASC) are close to MSC from bone marrow in their anti-inflammatory and supportive for tissue repair effect [5]. The multipotent differentiation abilities [6] as well as accessibility, reproducibility, and ease of isolation of ASCs make them ideal candidates for musculoskeletal repair, and a number of ASC-based approaches for cartilage repair have progressed from preclinical animal studies into clinical trials [7]. There...

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